Compulsive eating behavior is a transdiagnostic construct that shares many behavioral, neurobiological, and theoretical features with compulsive drug use. The focus of this dissertation is to progress a framework for compulsive eating behavior, including identification of risk factors for its development and examination of functional neuroadaptations to brain reward systems in an animal model of compulsive eating.
We first investigated impulsivity (impulsive choice and impulsive action) as a potential vulnerability factor for the development of binge and compulsive eating behavior. Impulsivity has been implicated in drug addiction as well as eating disorders and obesity, but its exact role in the conferment of risk for compulsive eating is unknown. To achieve this, we measured impulsive choice (i.e. delay discounting) and impulsive action (i.e. motor impulsivity) and subsequent binge-like eating. We observed no effects of impulsive choice behavior on binge-like eating of palatable food; however, impulsive action predicted higher binge-like eating, higher motivation for palatable food, and increased compulsive-eating behavior. Therefore, impulsive action, but not impulsive choice, predicted the development of binge- and compulsive-like eating behaviors.
The second aim of this dissertation was to investigate functional neuroadaptations to brain reward pathways in rats with a history of palatable diet alternation, a model of compulsive eating. Overeating of palatable food, similar to exposure to drugs of abuse, is hypothesized to cause reward deficits via downregulation of mesolimbic dopamine systems. To investigate this, we measured sensitivity to d-Amphetamine using behavioral and neurochemical methods. To identify potential neuroadaptations to the dopamine and dopamine transporter (DAT) systems, we assessed baseline NAc-shell dopamine and DAT function in vivo. In rats with a history of palatable diet alternation, we observed deficits in the stimulating, reward-enhancing, and rewarding effects of d-Amphetamine, and impaired d-Amphetamine-induced dopamine efflux in the NAc-shell. Furthermore, dopamine and dopamine transporter systems were downregulated evidenced by decreased extracellular NAc-shell dopamine at baseline and decreased DAT function.
These results contribute to an overall framework for compulsive eating behavior where initial impulsivity predisposes compulsive eating and compulsive eating results in the emergence of reward deficits. / 2021-06-14T00:00:00Z
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/36684 |
| Date | 14 June 2019 |
| Creators | Moore, Catherine Frances |
| Contributors | Cottone, Pietro |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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